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The Neurophysiology Of Golf Putting:
The Mayo Clinic Takes a Stab at the "Yips"

Geoff Mangum

The PuttingZone, Greensboro NC USA 27401. Email: geoff@puttingzone.com

ABSTRACT: The Mayo Clinic is undertaking a study of the "yips" in golf--the mysterious affliction in putting manifested by freezing over the putt, shaky hands, and a stabbing stroke. Previous researchers have classified yips as an occupational focal hand dystonia, a type of movement disorder apparently caused by degeneration of neural circuitry following decades of the same hand movement. The Mayo Clinic team departs from earlier researchers by assigning a prominent role in the etiology of the yips to psychological rather than neurological factors. They have also opted for a behavioral definition of yips that does not distinguish between the contributions of anxiety and dystonia. The team may therefore have difficulty identifying effective therapy. (Nov. 2002).

"Once you've had 'em, you've got 'em" - Henry Longhurst

A movement disorder long known to interfere with putting, the "yips" affect between one-fourth and one-half of all mature golfers (Smith et al., 2000). The Sports Medicine Center of the Mayo Clinic in Rochester, Minnesota, is heading up a multidisciplinary team studying the yips in golf (Smith et al., 2000; Mayo Clinic, 2000). The study focuses on anxiety and neuromuscular movement disorders that have wide applicability to other sports.

The study team does not distinguish by clear clinical criteria between neuromuscular movement disorders and neuropsychological processes responsible for anxiety deficits in sports performance. Relying on 1,031 responses to a detailed questionnaire from skilled, low-handicap Minnesota golfers, plus a small pilot study of the physiology of seven respondents during putting, the team investigated anxiety and putting performance. The team's preliminary report concluded that the yips consist of a continuum of disorders from the psychology of choking at one extreme to a strictly neurological deficit (occupational focal hand dystonia) at the other. The team believes that the majority of afflicted golfers suffer from a mixed psycho-neurological form of the yips between these extremes (Smith et al., 2000). Studies of additional golfers are planned for the World Golf Village in St Augustine, Florida (Mayo Clinic, 2001). The working definition of the "yips" used by the Mayo Clinic unfortunately confounds anxiety and neuromuscular deficits by relying upon behavioral rather than clinical characteristics.

In this article, I will review the two previous studies of the yips as well as the neurophysiology of anxiety and dystonia. I will then offer a critique of the Mayo Clinic study suggesting the need for a more rigorous dissociation of anxiety-sponsored and dystonia-sponsored movement deficits, in terms of clinical signs and symptoms rather than behavioral characteristics of the yips, as generally understood. I argue that a deeper understanding of the distinct neuropsychology and neurophysiology of anxiety and dystonia is necessary before effective therapeutic approaches can be identified.

The Yips in Popular Parlance

The putting condition was known from the early 1900s as "the jumps" and "whiskey fingers" (Golf Dig. 1968; Golf Dig. 1973; Vardon 1912). In the 1920s, the word yips was confined popularly to an obscure people dwelling in L. Frank Baum's fictional land of Oz.

During the 1940s, the putting affliction was called "the jitters" (Boros, 1968; Golf World, 1949), a term associated with "jitterbug," meaning a drunk with palsied tremors (Dictionary.com, 2001). The term yips in reference to golf putting originated around 1963 (OED, 1989; Times, 1963) and was given wider currency in Tommy Armour's ABCs of Golf, where he describes the difficulties that led him to abandon tournament play (Armour, 1967; Longhurst, 1973).

The present-day term covers a broad spectrum of behaviors:

Numerous famous professional golfers have been afflicted, including Harry Vardon, Bobby Jones, Ben Hogan, Sam Snead, Bernhard Langer, and Sam Torrance (Palmer and Dobereiner, 1986). Traditional therapies have featured switching to the long putter or other modifications of putting stroke technique (Moody and Van Kampen, 1990).

Most golf instruction gurus, golf psychologists, and golfers in general believe that the yips are a psychological problem with a psychological cure (Anthony, 2001; Cohn, 2000; Leadbetter, 1993; Pelz, 2000; Rotella, 1995). Only a minority in golf acknowledges the neurological basis of the disorder (Palmer and Dobereiner, 1986; McLean and Pirozzolo, 1994). The term is variously applied to different forms of dysfunction. Many golfers are described as suffering from the yips, when instead the golfer may simply be in an extended slump attributable to unreliable technique or skill, such as the notorious putting slumps of Arnold Palmer, Johnny Miller, Hal Sutton, Tom Watson, and Nick Faldo. Other golfers are said to have the yips when they are simply struggling to master the art of putting, experiencing many fluctuations in their success (e.g., Vijay Singh, whose steady improvement over the last several years now ranks him near the top in professional putting). And golfers who miss short putts in dramatic tournament settings are also said to have "yipped" the putt (e.g., Scott Hoch, Ed Sneed, Doug Sanders; see Barkow et al., 1998). The term has also gained currency in other sports for a spoiled shot or stroke, as in rugby, soccer, cricket, and tennis (Happell, 2000; Google.com, 2001; Leonard, 2000; McAsey, 2002; Taylor, 2000).

Previous Studies of Putting Yips

Two previous studies have concluded that the yips in putting are a neuromuscular disorder in the class of occupational focal hand dystonias that includes writer's cramp, pianist's fingers, and other forms associated with long-term repetition of skilled hand movements (McDaniel et al., 1989; Sachdev, 1992). Researchers at the West LA Medical Center in 1989 gathered questionnaire data from 1,050 professional and amateur golfers (McDaniel et al., 1989). An Australian study three years later examined the clinical characteristics of 20 Australian golfers with the yips against control golfers (Sachdev, 1992). Both studies framed the issue in terms of whether the yips were caused by anxiety or whether anxiety simply accompanied and exacerbated a neuromuscular disorder.

According to these studies, yips-affected golfers reported anxiety at about the same level as non-affected golfers, and there was no difference in the frequency or severity of anxiety-related symptoms between the two groups. The authors concluded the yips are not caused by anxiety or psychogenic in origin (although often accompanied by dread or fear), but instead have a neurogenic pathophysiology. Even though data indicates yips-affected golfers rate themselves as more anxious than non-affected golfers, and 77% of affected golfers believe the severity of performance deficits is proportional to subjective anxiety levels, the authors agreed these subjective beliefs were by-products of the neuromuscular disorder rather than a cause (MacDaniel et al., 1989; Sachdev, 1992).

Neuroscience of Occupational Focal Hand Dystonia

These earlier putting studies are in line with modern neuroscience, in which occupational focal hand dystonia is only imperfectly understood (Hochberg et al., 1990; Wake Forest Neurosurgery, 2001), but is no longer considered to be psychological in origin (e.g., Abbruzzese et al., 2001; Adler, 2000; Hallett, 1998; Hochberg et al., 1990; Sheehy and Marsden, 1982). Classed as a movement disorder along with Parkinson's Disease, cortico-basal degeneration (CBD), and various forms of spasticity (Dystonia Medical Research Foundation, 2001; We Move, 2001), focal hand dystonia has been linked with:

Furthermore, occupational focal dystonias are not restricted to the hands (e.g., "auctioneer's jaw": Scolding et al., 1995).

The emerging picture is of a complex loop of brain centers integrating perception, emotion, and movement that is subject to disruption at varying points with resulting movement deficits that can be quite similar. For example, vestibular dysfunction contributes to spasmodic torticollis (a related dystonia; Munchau et al., 2001); cervical spinal lesions can produce dystonia-like deficits in hand movements without involvement of cerebral circuits (Uncini et al., 1994); and cerebellar degeneration results in excess cortical activation in motor control (Liepert et al., 2000). Focal hand dystonia is considered mostly intractable, but limited relief can be gained from periodic injections of the hand muscles with botulinum toxin A (Naumann and Karlheinz, 1997; Poungvarin et al., 1995). In addition, brain surgery with thalamotomies (lesioning of the basal-cortico motor control loop at a point in the thalamus) has been effective (Kelly, 2001; Mempel et al., 1986).

Neuroscience of Anxiety Disorders

The American Psychiatric Association recognizes four broad classes of anxiety disorders: panic, phobia, obsessive-compulsive, and generalized anxiety disorders (American Psychiatric Assoc., 1994). Golfers tend to speak very broadly of "pressure," "stress," "anxiety," "fear," and similar terms without careful definitions. "Anxiety" is too often used to cover a wide variety of mental and neuropsychological states. In particular, current neuroscience distinguishes "defensive avoidance" in the amygdala circuitry from "defensive approach" in the septo-hippocampal circuitry. The former is related to fear, panic, phobia, and flight behavior, and the latter to generalized anxiety and dread or "anticipatory frustration" (Gray and McNaughton, 2000; LeDoux, 1992; LeDoux, 1996 ). These dissociations of the underlying neurology and the forms of anxiety-related responses represents a more complex view of the traditional "fight-flight" reaction in light of recent neuroscience.

The therapeutic efficacy of anti-anxiety psychopharmaceuticals (anxiolytics such as beta-blockers and tranquilizers) depends upon these underlying structural differences (Gray and McNaughton, 2000). For example, the amygdala system mediates fear and phobia and generates panic and flight behavior, whereas the septo-hippocampal network mediates dread and anticipatory frustration and generates hesitation and vacillation behaviors. While the amygdala system responds to panicolytic drugs with relief of behavioral signs, it is not directly responsive to anxiolytic drugs. The septo-hippocampal system, on the other hand, is responsive to anxiolytics but not to panicolytics. Classical anxiolytics include ethanol, barbiturates, and benzodiazepines, but their side effects mask locating the affected neural structures . The new class of anxiolytics developed in the last decade, especially busiprone, has the advantage of working to reduce anxiety without the side effects of the benzodiazepines or the addictive toxicity of ethanol and barbiturates. Clinical observation of the efficacy of this new class of drugs allows much clearer identification of the neural structures mediating anxiety. (Gray and McNaughton, 2000).

The neurophysiology of the so-called stress response is naturally closely connected with the fear-anxiety mechanisms in the amygdala and hippocampal circuitry. The autonomic fight-flight response in the sympathetic nervous system is the stress-induced mechanism whereby the adrenal gland readies the body's muscular, cardiovascular, immune, and nervous systems for aggression, escape, and possible injury under conditions of real or imagined threat or danger (Hadley, 1996; Stanford and Salmon, 1993; West 1990). Two neural subsystems activate this stress response: the anterior pituitary adrenal cortex system (elevating blood levels of glucocorticoids, which forms the most common physiological measure of stress) and the hypothalmic-adrenal medulla system (elevating blood levels of epinephrine and norepinephrine) (Pinel, 1997; Shier et al., 1999). In both cases, the adrenal systems are activated by signals from the hypothalamus, which in turn is initially recruited by the amygdala (Davis, 1992). The form of anxiety mediated by the hippocampal circuitry also activates the hypothalmic-adrenal system (probably via the amygdala), but does so in a manner inhibiting and moderating the behavioral outputs of the stress response (Gray and McNaughton, 2000). The behavioral basis, then, for detecting whether the underlying neurology is principally fear-based (amygdala) or anxiety-based (hippocampal) is a matter of intensity of physiologic reaction. Consequently, the outward behavioral signs of the stress response may appear similar for differing underlying neural mechanisms, but pharmacological treatments have different effects depending on the differing mechanisms (Gray and McNaughton, 2000).

The Mayo Clinic Departure from Earlier Yips Studies

The Mayo Clinic study differs significantly from the earlier yips studies. The Mayo Clinic team finds the neurological disorder and anxiety closely related (Smith et al., 2000). Following the path of the West LA Medical Center and Australian studies, the Mayo Clinic team states its objective: to determine whether anxiety-related stress exacerbates the condition or in some way brings about the neurological pathology (Smith et al., 2000). At issue is whether anxiety produces neuromuscular disorder. The related issue of whether the neurological disorder produces anxiety is not explicitly discussed but is tacitly assumed in the discussion.

The earlier studies found no causal relation between anxiety and dystonia, but the Mayo Clinic team appears to reject this finding. The key difference in analysis is that the Mayo Clinic team believes episodic anxiety in golf can produce dystonia-like performance deficits over time. From this proposition, the team credits a prominent but not total causal role for anxiety in the yips. The team hence aligns itself with anecdotal accounts of golfers and the prevailing lore of the yips among golf's sports psychologists and gurus who reject the neurological underpinnings of the phenomenon in favor of a psychological explanation.

What is unclear about the Mayo Clinic study is whether anxiety is being blamed as a cause for yips behavior or for dystonia itself. The study team implies that anxiety somehow causes dystonia, but the precise mechanism of the supposed causation is not examined (Smith et al., 2000). Instead, the team collects together behavioral effects from reports and observations of behaviors thought to represent the yips and loosely associates the whole with anxiety, dystonia, or some combination of the two.

The Yips Study and "Choking" Studies

The Mayo Clinic team includes Dr Debbie Crews from the Department of Exercise Science at Arizona State University (Crews, 2001). The Mayo Clinic position on the yips apparently builds upon other studies by Dr Crews on "choking" under pressure in golf and on attentional patterns in putting (Crews and Landers, 1993). Choking is generally understood to refer to anxiety-sponsored increases in arousal level that lead to performance deficit, typically associated with failure in informal situations or in high-pressure competition. The 1996 experience of Greg Norman at the Masters in losing a final-round six-shot lead to Nick Faldo prompted the NBC program Dateline to bankroll a study of choking in golf by Dr Crews and others. This research consisted of an EEG study of ten amateur golfers with an average golfing experience of five years, and with handicaps ranging from 11.5 to 26. The task was a trial of 20 five-foot putts for baseline, followed by a second trial of 20 putts on condition that the golfers who improved won $300 while golfers who performed worse than baseline would have to pay $100. Five did better, and five did worse (Linder et al., 1998; Abrahams, 2001).

Basing her analysis of choking upon comparative EEG patterns, Dr Crews concluded that successful golfers had increased cortical activity just like unsuccessful golfers, but the activation was spread evenly over both hemisphere of the brain, whereas activation for unsuccessful golfers concentrated in the left (dominant) hemisphere (Abrahams, 2001). Dr Crews interpreted the increased left-brain EEG activity as anxiety-related and interpreted the successful golfer's brain pattern under pressure as the consequence of employment of right-brain processes. In keeping with this analysis of handling pressure, Dr Crews teaches "right-brain" golf by encouraging golfers to use imagery, relaxation techniques, and target focus as ways to promote right-brain activation and therefore hemispheric balance. This research was awarded the First Annual Golf Science award from Golf Magazine and the World Scientific Congress on Golf.

The concept of anxiety and physiological research methodology followed in the Mayo Clinic study is closely similar to that utilized by Dr. Crews in her "choking" studies (Smith et al., 2000). While the Mayo Clinic protocol in obtaining EMEG data from the seven subjects does not include the simulation of pressure, the EMEG data acquisition and analysis is the same as in the choking study. And the behavioral aspects of anxiety are also similarly identified (heart rate increase and higher level of cortical excitation associated with anxiety).

Criticisms of the Mayo Clinic Approach

The principal criticism of the Mayo Clinic approach is failure to separate anxiety and dystonia according to clinical criteria. The underlying neurophysiological processes of anxiety and dystonia are distinctly different (Gray and McNaughton, 2000; Hallett, 1998). Anxiety is generally categorized as a normal psychological state that may extend into pathological forms (with well-recognized physiological signs such as cardioacceleration, forced breathing, and mind blanking) (American Psychiatric Assoc., 1994), but focal hand dystonia is a neurological dysfunction with specific neurophysiological abnormalities (Hallett, 1998).

Instead of clinical criteria for anxiety or dystonia, the Mayo Clinic team uses self-reporting of behavioral characteristics of the yips. The team uses four criteria to assess whether subjects are affected:

Golfers are then rated according to how many criteria they self-report. Only 200 respondents gave sufficient information to be rated. Of these 136 (68%) met 3 or 4 of the criteria. Actual physiological data during putting was gathered only from seven respondents, measuring heart rate (ECG), grip force (GF), and muscle activation patterns (EMEG). Of these, only four self-reported as yips-affected, but the criteria rating was not reported for these subjects. The seven golfers were then monitored for heart rate, grip pressure, and EEG brainwave muscle activation patterns during putting. The four affected golfers exhibited higher heart rates, grip force, and EMEG excitation than non-affected golfers. While the data allow dissociation of these four golfers from non-affected golfers in terms of the physiological signs, the physiological data fail to discriminate between effects due to anxiety versus neuromuscular dysfunction.

The criteria for defining which golfers are yips-affected conflate anxiety and dystonia by focusing on yips behavioral rather than the distinct clinical signs and symptoms of anxiety and dystonia. The team's working definition of the yips in these terms of behavior effectively precludes separating out the contributions of the two from a neurophysiological perspective. It should be possible to identify golfers suffering solely from anxiety-related performance deficits and golfers suffering solely from neuromuscular-related deficits unattended by anxiety, with appropriate clinical symptomatology.

For example, inasmuch as hand dystonia correlates with somatosensory degradation in cortical representations of the hand and fingers (Byl et al., 2000), one possible clinical sign of hand dystonia is an elevated threshold for detection of finger-prick probes administered in close temporal succession (Bara-Jimenez et al., 2000). Clearly, the pharmacological therapy for dystonia (periodic injections of botulinum toxin A into the hand muscles) has no direct effect on anxiety (Naumann and Karlheinz, 1997; Poungvarin, 1995). Similarly, the use of anxiolytic drugs to alleviate performance anxiety is very unlikely to have any influence upon dystonia-based motor control deficits (Gray and McNaughton, 2000). The Mayo Clinic team suggests future testing of anxiolytics to check the contribution of anxiety to what it terms yips-affected behaviors; if anxiolytics reduce or eliminate yips-affected behaviors, then anxiety would be credited with the principal causative role (Smith et al, 2000). On the other hand, if anxiolytics reduce signs and symptoms of anxiety and yet the yips-affected behaviors persist, then the dystonia would be blamed. Experiments carried out along these lines would certainly be a step in the right direction, but this promising approach remains to be undertaken.

The second overall problem is that the Mayo Clinic study lacks any sustained analysis of the neuropsychology or neurophysiology of anxiety or dystonia. Reports of yips behavior, including the dread of failure facing short putts (e.g., Longhurst, 1973), are more consistent with the septo-hippocampal system of anxiety from anticipatory failure than the panic-phobic behavior of the amygdala system. The septo-hippocampal system appears to mediate situations where the person is acting with conflicting goals and motives, such as the need to attempt a short putt to complete play on the hole versus dread of embarrassment at missing the putt. This is categorically different from the fear and phobic reactions that necessitate escape behavior without conflicting motivation. Assuming the septo-hippocampal system underlies yips anxiety, then the interference with motor programs is believed to have its telling effect via hippocampal neural projections to the basal ganglia (Gray and McNaughton, 2000). This common basal-ganglia connection between anxiety and dystonia may well support an overlapping of motor deficit symptoms, but the issue remains to be examined. Again, notwithstanding similarities in outward behavioral signs, the underlying neural mechanisms are distinct, and identification of appropriate treatments requires clinical tracking of these mechanisms.

In addition, anxiety-sponsored behaviors may exhibit a progressive course that simulates the progression of a neuromuscular disorder. Recurrence or intensification of yips behavior is a potentially confusing and unreliable indicator of the neuropathology. There is evidence that the anxiety response of the septo-hippocampal system becomes conditioned to repeated exposures to stimuli, reacting more strongly over time with a reduced threshold for activating stimuli. (Gray and McNaughton, 2000). Similarly, the "fight-flight" reaction, whereby release of adrenaline heightens arousal, adapts to repeated exposure to the stressful stimulus by producing greater release of adrenaline (Xie and McComb, 1998). Hence, an intensification of the anxiety-sponsored motor deficits can occur without regard to neuromuscular dysfunction. While on the one hand this observation suggests that yips behavior from anxiety may be as potent and outwardly similar as that derived from dystonia, on the other hand it underscores the need for non-behavioral signs to separate the phenomena.

A third criticism is that the Mayo Clinic team does not discuss anxiety-related performance deficit in terms of the arousal-performance dynamic expressed in the well-known Yerkes-Dodson law. This general law of sports psychology relates arousal level and task performance in an inverted-U relationship (Florida State University, 2000; Schmidt, 2001). There is presumably an optimal level of arousal for putting performance (perhaps specific to an individual but also determined by the complexity or difficulty of the immediate task) and anxiety-sponsored increases in arousal are likely to cause performance problems (Schmidt, 1991). But the relationship between stress and arousal is not quite that simple, as arousal can be beneficial in some situations, enhancing perceptual focus and acuity and promoting greater accuracy and responsiveness to environmental cues (Gray and McNaughton, 2000). These issues must be addressed in coming to terms with anxiety-related stress in sports performance.

The Question of Therapy or Cure

The Mayo Clinic study does not attempt analysis of treatment or cure for its description of yips behaviors. Instead, the team lists possible interventions for future study, including:


(Smith et al., 2000). Curiously, the Mayo Clinic team does not discuss the principal treatment for dystonia: the so-called "miracle poison - botulinum toxin" (Caviness, 2000; Jankovic and Hallett, 1994; Poungvarin et al., 1995). Such periodic injections are the "treatment of choice" for most forms of dystonia (Adler, 19999; Adler, 2000), The toxin works at the neuromuscular junction by blocking release of acetylcholine, the neurotransmitter responsible for muscle activation (Blais et al., 1993; Hobson, 2001). Although such treatments are considered safe and are used for eye-lid twitches and facial spasms (Adler, 2000), the use of botox injections for focal hand dystonia has limited success due to the complexity of muscular activation patterns involved in specific cases and must be tailored to the individual with EMG studies (Hobson, 2001). In addition, the use for hand treatments is practically limited due to a resulting weakness in hand and finger muscles (Evidente, 2000). While it is doubtful that many golfers would prefer to undergo this treatment due to hand-weakness effects not related to golf, the treatment should be discussed by the Mayo Clinic team. The treatment clearly indicates the non-psychological basis for the neuromuscular disorder, and as such serves to differentiate the psychological from the neurological etiology of yips behaviors.

Treatment programs must be tied to a specific diagnosis of the underlying psycho- or neurophysiology (Andrews et al., 1994). Individuals are treated, not ranges of dysfuction in general. Unless a specific individual's condition is diagnosed clinically, the "treatment" must proceed by trial-and-error under conservative management, as is typically the case when a family physician treats an unknown illness that may be caused by infection or biochemical imbalance or other unknown cause. The Mayo Clinic team's approach of testing a cafeteria-style selection of interventions is tantamount to acceptance of not being able to identify the underlying neurological processes - hence the "trial-and-error" approach. Instead, in order to diagnose and then treat a specific individual with reasonable scientific footing, the Mayo Clinic team must come to grips with the neurological differences between the array of phenomena they class collectively as "the yips." Only then can the specific treatment options be tailored to individual manifestations of dysfunction.

Because of the diverse and complex neurophysiological processes encompassed by anxiety and dystonia, disentangling the separate processes that underlie performance deficits collectively known as the yips is a necessary first step in identifying effective treatment. But experimental probing with various anxiolytic drug treatments known to affect distinct neural processes appears to be a promising approach.

Conclusion

The Mayo Clinic study affords a detailed look at the current understanding of the yips among golfers and golf scientists. However, the phenomena under examination must be observed separately by well-crafted experimental protocols for a deeper understanding of the controlling neurophysiological processes. Without this deeper understanding, effective therapy will likely remain elusive.

 

UPDATE AUG. 2004:

According to recent press releases and interviews, the Mayo Clinic after receiving the above paper has added Dr Charles Adler (Mayo Clinic neurologist and movement disorder specialist) to their team of investigators since the Sports medicine team first began their investigation, and they now have found that the Yips are neurological in the big majority of cases (whereas before they emphasized the psyhcological origins). Dr Adler and the team is still attempting ad hoc trial-and-error therapies without separating out the neurological yips from the psychological yips, and without getting down to the underlying etiology. Hence, their efforts to find a generally applicable, effective treatment do not look promising. -- Geoff Mangum, 13 Aug. 2004 ["There isn't much known about golfers' yips, so this is an important initial study," said Christine Klein, MD, in an interview seeking outside comment. "A common perception of the yips is that it's psychogenic, and Dr. Adler's work shows that it may be neurogenic instead." Dr. Klein is the Lichtenberg professor of clinical and molecular genetics at the University of Lubeck in Germany. Medscape Apr 2005.]

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